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Published on: February 6, 2018
Curcumin promotes spermatogenesis in mice with cryptorchidism by regulating testicular protein O-GlcNAcylation
Zhen Wang1, Fujia Chen1, Yun Li1
1School of Biological and Food Processing Engineering, Institute of Agricultural Products Fermentation Engineering and Application, Huanghuai University, Zhumadian, China.
Introduction:
Curcumin has garnered increasing attention in male reproductive research due to its potential anti-infertility properties. This study aimed to explore the protective effects of curcumin on spermatogenesis impairment in mice with cryptorchidism and to elucidate the underlying mechanisms.
Methods:
A total of 56 male Kunming mice aged 10 to 15 days were randomly assigned to different groups, including a control group (BO) and a cryptorchid group with five curcumin treatment groups (CC25, CC50, CC100, CC200, and CC300) receiving varying doses of curcumin (25, 50, 100, 200, and 300 mg/kg, respectively). After five weeks of treatment, evaluations based on organ coefficients, sperm count detection, testicular pathology analysis, and hormone level assessments determined the most effective curcumin dosage.
Results And Disccusion:
The findings indicated that cryptorchidism had a detrimental impact on reproductive function, evident by decreased testicular coefficient, cessation of sperm production, abnormal testicular tissue morphology, and hormonal imbalances. Curcumin treatment mitigated these abnormalities, with the most significant improvement observed at a dosage of 100 mg/kg, without substantial adverse effects on other organs. Mechanistic studies revealed that cryptorchidism reduced testicular protein O-GlcNAcylation levels, while curcumin supplementation effectively increased this modification in a dose-dependent manner. Molecular docking and UDP-GlcNAc analyses further demonstrated that curcumin restores O-GlcNAcylation homeostasis by inhibiting OGA via high-affinity binding and enhancing OGT activity through substrate accumulation, synergistically rebalancing O-GlcNAcylation dynamics. This study uncovers a novel mechanism by which curcumin facilitates spermatogenesis through the regulation of testicular protein O-GlcNAcylation, providing a significant theoretical foundation for its utilization in male reproductive health.
Insights
Curcumin supplementation improved male fertility in cryptorchid mice by restoring sperm production and testicular health. It works by regulating protein O-GlcNAcylation, a key mechanism for male reproductive health.
Area of Science:
- Reproductive Biology
- Endocrinology
- Pharmacology
Background:
- Male infertility is a growing concern, with cryptorchidism being a significant contributing factor.
- Curcumin, a natural compound, shows promise for male reproductive health, but its mechanisms are not fully understood.
Purpose of the Study:
- To investigate the protective effects of curcumin on spermatogenesis impairment in cryptorchid mice.
- To elucidate the underlying molecular mechanisms of curcumin's action.
Main Methods:
- Male Kunming mice were subjected to cryptorchidism and treated with varying doses of curcumin (25-300 mg/kg).
- Evaluations included organ coefficients, sperm counts, testicular pathology, hormone levels, and protein O-GlcNAcylation analysis.
- Molecular docking and UDP-GlcNAc analyses were performed to understand curcumin's interaction with key enzymes.
Main Results:
- Cryptorchidism impaired sperm production, testicular morphology, and hormone balance.
- Curcumin treatment, particularly at 100 mg/kg, significantly mitigated these negative effects.
- Curcumin restored testicular protein O-GlcNAcylation by modulating OGA and OGT activity, suggesting a novel therapeutic pathway.
Conclusions:
- Curcumin effectively protects against cryptorchidism-induced spermatogenesis impairment in mice.
- The study reveals a novel mechanism involving the regulation of testicular protein O-GlcNAcylation by curcumin.
- Curcumin holds potential as a therapeutic agent for male infertility, particularly related to oxidative stress and impaired spermatogenesis.
